FOXA2 Mouse Monoclonal Antibody
- Known as:
- FOXA2 Mouse Monoclonal Antibody
- Catalog number:
- BIN-003170-M10
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FOXA2 Mouse Monoclonal Antibody
Related genes to: FOXA2 Mouse Monoclonal Antibody
- Gene:
- FOXA2 NIH gene
- Name:
- forkhead box A2
- Previous symbol:
- HNF3B
- Synonyms:
- -
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-11
- Date modifiied:
- 2016-10-05
Related products to: FOXA2 Mouse Monoclonal Antibody
Related articles to: FOXA2 Mouse Monoclonal Antibody
- Despite decades of biochemical and structural studies of the nucleosome, researchers lack genome-scale methods to determine variability in nucleosome structure along individual chromatin fibres. To address this, here we present Iteratively Defined Lengths of Inaccessibility (IDLI), a computational method that maps the single-molecule co-occupancy of structurally distinct nucleosomes, subnucleosomes and other protein-DNA interactions through long-read single-molecule footprinting. IDLI classifies methylase-inaccessible footprints on individual chromatin fibres into (i) linker-histone-associated nucleosomes; (ii) nucleosomes with focal DNA accessibility along the nucleosome wrap; (iii) unwrapped nucleosomes; and (iv) subnucleosomal species such as hexasomes, tetrasomes and other short DNA protections. Applying IDLI to chromatin from mouse embryonic stem cells, we discover that more than 85% of nucleosomes exhibit intranucleosomally accessible DNA (nucleosome 'distortion'). We observe epigenomic-domain- and expression-level-specific patterns of distortion, including at promoters and mouse satellite repeat sequences. Transcription factor (TF) motif occurrence correlates significantly with distinct types of distortion, and degron experiments provide evidence of direct regulation by TFs. We apply IDLI to in vitro endoderm differentiation in human induced pluripotent stem cells and primary mouse hepatocytes. In both cases, we observe distortion at pioneer TF FOXA2 binding sites, demonstrating that distortion is developmentally encoded and present in vivo. Finally, genetic experiments in mice show that a nucleosome-binding domain of FOXA2 directly affects nucleosome structure in vivo, implicating these protein-nucleosome interactions as direct mediators of distortion. Our work suggests extreme but regulated nucleosome structural variability at the single-molecule level. Furthermore, our approach offers opportunities to model TF binding, nucleosome remodelling and cell-type-specific chromatin regulation across biological contexts. - Source: PubMed
Publication date: 2026/04/29
Yang Marty GRichter Hannah JWang SimaiMcNally Colin PMoore Camille MEmadi AliHarris Nicole EDhillon SimaronMaresca MichelaPan HuiminSaunders HaydenYang RuiqiaoOstrowski Megan SAnderson Erika Cde Wit ElzoMaher Jacquelyn JFan YuhongNarlikar Geeta JNora Elphège PWillenbring HolgerGoodarzi HaniRamani Vijay - Prostate cancer, particularly metastatic castration-resistant prostate cancer (mCRPC), presents therapeutic challenges rooted in adaptive lineage plasticity and neuroendocrine transdifferentiation. Conventional genome-based models fail to account for the divergent clinical trajectories observed among tumors that share identical driver mutations. This limitation requires reconceptualizing cancer as a dynamic system in which tumor cells can execute context-dependent molecular programs governed by epigenetic and transcriptional network remodeling. This review critically evaluates three convergent technological pillars reshaping prostate cancer research and clinical care. First, conditional reprogramming (CR) enables the rapid generation of patient-derived models that preserve genomic fidelity, intratumoral heterogeneity, and reversible phenotypic plasticity without genetic manipulation. Second, single-cell and spatial multi-omics approaches have clarified the cellular trajectories underlying luminal-to-neuroendocrine transdifferentiation, identifying a therapeutically actionable intermediate state. They have revealed the hierarchical transcription factor network (FOXA2-NKX2-1-p300/CBP) which orchestrates chromatin remodeling during this lethal transition. Third, physics-informed machine learning and digital twin architectures aim to move beyond correlative risk prediction toward mechanistically sound forecasting of tumor evolution, treatment response, and resistance emergence. We address unresolved challenges in prospective clinical validation, spatial heterogeneity capture, regulatory pathways for functional diagnostics, and the imperative for causal, as opposed to associative, inference from perturbational datasets. The integration of these three domains through closed-loop experimental-computational feedback cycles represents a paradigm shift from reactive to anticipatory precision oncology. - Source: PubMed
Publication date: 2026/04/15
Fadiel AhmedMalpani PunitEichenbaum Kenneth DNaftolin FrederickHassouneh AyaChong GeralynOdunsi Kunle - Adolescent idiopathic scoliosis (AIS) is a complex spinal deformity characterized by three-dimensional curvature of the spine with an unknown etiology. Previous genome-wide association studies have identified a single-nucleotide polymorphism (rs6137473) located downstream of which is significantly associated with female AIS risk. - Source: PubMed
Publication date: 2026/04/22
Moody Edward CWade Emma MMizumoto ShujiMcCallum-Loudeac JeremyWilson Megan J - Diabetes mellitus, characterized by β-cell dysfunction and loss, results in impaired insulin secretion and chronic metabolic complications. Mesenchymal stem cells represent a promising source for β-cell regeneration owing to their endodermal differentiation potential. This study optimized the differentiation of human tonsil-derived mesenchymal stem cells (TMSCs) into pancreatic β-like cells through the comparative evaluation of two signaling-based protocols. - Source: PubMed
Publication date: 2026/04/22
Yang JiinKim Ha YeongKim So JeongKim Han Su - Lung cancer remains a leading cause of cancer-related mortality, largely due to its complex immune microenvironment and molecular heterogeneity. To address gaps in understanding tumor heterogeneity and the role of long non-coding RNA (lncRNA) macromolecules, we conducted an integrative single-cell RNA sequencing (scRNA-seq) analysis of non-small cell lung cancer (NSCLC). Unsupervised clustering identified distinct immune and malignant cell populations. Differential expression analysis identified robust cell-type markers, including novel lncRNA macromolecules, AC005842.1, AC009041.2, and AC007240.1 enriched in specific tumor and immune subsets. Functional enrichment linked these lncRNAs to key cancer pathways, including epithelial-mesenchymal transition (EMT), hypoxia, and immune modulation. Targeted experimental validation using quantitative real-time PCR (qRT-PCR) in NSCLC cell lines confirmed significant upregulation of the identified lncRNAs and supported activation of EMT-associated molecular programs. Pseudotime trajectory modeling uncovered dynamic activation of hallmark programs, notably TNFA-NFκB and IL2-STAT5 signaling, suggesting progressive immune suppression and metabolic reprogramming during tumor evolution. We further identified novel transcription factor-pathway associations, including NR5A1-OXPHOS (oxidative phosphorylation) and FOXA2-mTORC1, pointing to uncharacterized axes of macromolecular regulation. To ensure reproducibility and accessibility, we developed lncScape, a modular, open-source Shiny application for integrative lncRNA analysis in single-cell datasets. lncScape implements a pipeline for clustering, lncRNA detection, pseudotime modeling, and GSVA-based pathway enrichment. It also introduces two novel scoring strategies the lncRNA Dynamics Score (LDS) and TF-lncRNA Dynamics (TLD) to prioritize dynamic regulatory lncRNAs based on expression patterns and transcription factor associations. Our findings expand understanding of lncRNA macromolecules in lung cancer and provide a practical platform for lncRNA-centric research. - Source: PubMed
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Haider AliDin Rahman UdHabib BushraLi Chunhua